Showing papers on "Hyperdynamic circulation published in 1989"

Beneficial effect of 8-ornithin vasopressin on renal dysfunction in decompensated cirrhosis.

Abstract: In nine patients with decompensated alcoholic cirrhosis of the liver and impaired renal function the effect of 8-ornithin vasopressin (ornipressin) on renal function and haemodynamic parameters was studied. Ornipressin was infused at a dose of 6 IU/h over a period of four hours. During ornipressin infusion an improvement of renal function was achieved as indicated by an increase of creatinine clearance (76 (15)%; p less than 0.01), urine volume (108 (29)%; p less than 0.05) and sodium excretion (168 (30)%; p less than 0.05). The hyperdynamic circulation of hepatic failure, as characterised by increased cardiac index and heart rate as well as decreased systemic vascular resistance was reversed to a nearly normal circulatory state during ornipressin infusion. The raised noradrenaline plasma concentration (1.74 (0.31) ng/ml) and plasma renin activity (13.5 (3.9) ng/ml/h) were lowered during ornipressin infusion to 0.87 (0.21) ng/ml and 5.9 (2.1) ng/ml/h, respectively (p less than 0.01). The efficacy of a vasoconstrictor agent in reverting a hyperdynamic state and improving renal function provides evidence for the substantial role of accumulation of vasodilator substances and subsequent activation of sympathetic nervous system and renin-angiotensin-axis in the pathogenesis of renal dysfunction in hepatic failure. Values are expressed as mean (SE).

Hemodynamic Changes and Intravascular Hydration State in Heat Stroke

Abstract: Acute and serial hemodynamic measurements in 13 pilgrims (average age, 55.2 ± SD 9.3 years) suffering from heat stroke (average rectal temperature, 41.3 ± 1.0°C) revealed a hyperdynamic circulation...

Differential effects of antihypertensive drugs on nutritive and nonnutritive blood flow in anaesthetized rabbits.

Abstract: Arteriovenous (AV) shunt vessels connect arterioles directly to the venous side. These vessels play a role in thermoregulation and in the pathophysiology of migraine. Tracer microspheres are excellent tools to study drug effects on AV anastomoses. Microspheres with a diameter of 15 microns are unable to pass through capillary vessels, but they readily cross AV shunt vessels and are transported to the lungs and trapped there. We investigated the effects of antihypertensive agents on AV shunt flow in anaesthetized rabbits and we also measured nutritional blood flow in the ear, an organ known to have both nutritional and AV shunt vessels. Nitroprusside sodium tended to increase and prazosin strongly increased AV shunt flow. The calcium antagonist isradipine, by contrast, decreased AV shunt flow even though it is also a vasodilator. Spirapril, an angiotensin-converting enzyme inhibitor, elicited similar effects. The centrally acting antihypertensive agent guanfacine strongly decreased AV shunt flow. These effects did not correlate with the drug effects on nutritional blood flow, which were, however, so variable that none of them reached statistical significance. The following trends were seen: nitroprusside sodium, isradipine, and guanfacine increased nutritional blood flow, but prazosin, a dilator of AV shunts, did not. The amount of blood crossing through AV shunts from the arterial to the venous side is considerable (up to 15% of cardiac output before drugs). A drug-induced increase is not associated with an apparent benefit but causes a hyperdynamic circulation that might contribute to the hemodynamic load of the heart.

Pathophysiology and Epidemiology of Portal Hypertension

Abstract: Changes in portal pressure are regulated by changes in hepatic vascular resistance, which is normally under neurohumoral control, and portal tributary blood flow. Two theories on the pathophysiology of portal hypertension have been proposed: the ‘backward flow’ theory, in which portal hypertension is attributable to increased resistance to portal venous flow, and the ‘forward flow’ theory, in which increased splanchnic blood flow maintains portal hypertension despite extreme portal-systemic shunting. The sinusoidal abnormalities caused by an accumulation of collagen in the perisinusoidal space of Disse may induce increased resistance to blood flow in various pathological conditions of the liver. Non-cirrhotic portal hypertension results from not only relatively uncommon disorders prevalent mainly in Asia and tropical countries, but also from acute and chronic phases of relatively common liver diseases. Systemic hyperdynamic circulation, characterised by an increased cardiac output and a reduced peripheral vascular resistance, and splanchnic hyperaemia may develop as consequences of portal hypertension. Although the mechanisms of these changes are not clearly understood, portal-systemic shunting as well as some vasoactive substances, including prostaglandins, may be involved. The erosive and eruptive mechanisms are the two potential explanations for variceal bleeding. In the latter, pressure should not be viewed in isolation and other additive factors such as variceal size may be involved. Several new techniques of measuring variceal pressure and blood flow may improve understanding of the actual pathophysiology of variceal bleeding. Renal haemodynamic alterations secondary to the systemic circulatory changes produced by portal hypertension may occur. The geographical pattern of prevalence in disorders associated with portal hypertension is briefly described in this paper.

Cardiopulmonary changes occurring with pulmonary intravascular clearance of live bacteria in sheep.

Abstract: Sheep were infused with live bacteria to determine if the bacteria are phagocytized in the pulmonary circulation and to study the associated cardiopulmonary changes. Unanesthetized animals (n = 9) with chronic hemodynamic and pulmonary lymph catheters received a 1 hr central venous infusion of live Pseudomonas aeruginosa (5 x 10(7) Ps./minute) and were compared to a sham group (n = 7). The pulmonary arterial levels of bacteria were five to 100 times higher than the aortic levels. Pulmonary intravascular clearance rates were 79-91%. Electron microscopy of the lungs 24 hr after the bacterial infusion showed that pulmonary intravascular macrophages and neutrophils phagocytosed the bacteria. Severe initial and mild persistent pulmonary hypertension occurred. The pulmonary lymph flow was elevated, initially from hydrostatic pressure and later from increased permeability. A hyperdynamic circulation occurred from 6 to 18 hr, with elevated cardiac index and lowered systemic vascular resistance and mean arterial pressure, mimicking cardiopulmonary changes seen in clinical sepsis. The removal of bacteria in the lungs may contribute to the injury in sheep.